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Genetic variation of ten Norway spruce (Picea abies (L.) Karst.) clones regarding their decay resistance against brown rot fungi, as well as physical and chemical properties of clones were investigated. 31- year-old spruce clones: 26, 31, A10, A15, A7, B10, B15, B6, V7, V9 were selected across Latvia. The stem diameters of spruce clones varied between 13.0 and 20.9 cm. The wood density of clones ranged from 361 to 443 kg/m3. Klason lignin content, depending on the clone, was between 27.0%-28.9%. Cellular UV microspectrophotometry of the non-infected tracheids displayed the typical lignin distribution with highest absorbance values in the cell corners (abs280 nm 0.80) and compound middle lamellae (abs280 nm 0.48), while secondary wall showed lower lignin absorbance values (abs280 nm0.29 - 0.35). The deposition of phenolic extractives in ray parenchyma and epithelial cells of resin canals were emphasized by a significantly higher UV-absorbance (abs280 nm 0.68 to 0.78) when compared to the cell wall associated lignin. The content of acetone-soluble extractives of spruce clones varied between 1.1% - 1.8%. The x-value (natural durability) for all spruce clones after exposure to C. puteana and P. placentawas >0.90 (durability class 5, not durable). Most of clones after degradation by G. trabeum had x-value > 0.90 with exception of clones B15 and V9 that showed x-value ≤ 0.90 (durability class 4, slightly durable). Natural durability of spruce clones did not correlate with stem diameter, density, content of lignin and extractives.

In our study, early period degradation (10 days) of Scots pine (Pinus sylvestris L.) sapwood by the brown-rot fungus Coniophora puteana (Schum.: Fr.) Karst. (BAM Ebw.15) was followed at the wood chemical composition and ultrastructure-level, and highlighted the generation of reactive oxygen species (ROS). An advanced decay period of 50 days was chosen for comparison of the degradation dynamics. Scanning UV microspectrophotometry (UMSP) analyses of lignin distribution in wood cells revealed that the linkages of lignin and polysaccharides were already disrupted in the early period of fungal attack. An increase in the lignin absorption A(280) value from 0.24 (control) to 0.44 in decayed wood was attributed to its oxidative modification which has been proposed to be generated by Fenton reaction derived ROS. The wood weight loss in the initial degradation period was 2%, whilst cellulose and lignin content decreased by 6.7% and 1%, respectively. Lignin methoxyl (-OCH3) content decreased from 15.1% (control) to 14.2% in decayed wood. Diffuse reflectance Fourier-transform infrared (DRIFT) spectroscopy corroborated the moderate loss in the hemicellulose and lignin degradation accompanying degradation. Electron paramagnetic resonance spectra and spin trapping confirmed the generation of ROS, such as hydroxyl radicals (HO∙), in the early wood degradation period. Our results showed that irreversible changes in wood structure started immediately after wood colonisation by fungal hyphae and the results generated here will assist in the understanding of the biochemical mechanisms of wood biodegradation by brown-rot fungi with the ultimate aim of developing novel wood protection methods.

Brown rotted Scots pine (Pinus sylvestris) sapwood was studied using scanning UV microspectrophotometry. Wood blocks were exposed to the fungus Coniophora puteana (Schum.: Fr.) Karst. (BAM Ebw.15) for 6, 8, 10, 30, and 50 days. No wood weight loss was detected in the initial decay periods. On the other hand, point analyses of lignin distribution in wood cells revealed higher absorbance after 6–10 days of decay, which we interpret as an increase in the absorption coefficient of lignin due to its oxidative modification by the fungus. Uneven wood degradation occurred in the later periods (30 and 50 days), with both significantly decayed and visually sound cells observed. The decayed cells showed a higher absorbance at 280 nm, although the apparently sound cells were also degraded to a lower extent. Degradation of lignin-rich compounds in middle lamellae and cell corners was not observed during fungal attack.